CLINICAL COMMUNICATION TO THE EDITOR
‘Atypical Pneumonia’: Acute Mitral Regurgitation Presenting with Unilateral Infiltrate
Acute mitral regurgitation is a medical and surgical emergency. It rapidly leads to cardiogenic shock and death if not promptly treated.1
where he was intubated due to worsening hypoxia. He also required 5 vasopressors for blood pressure support. Due to the refractory nature of his shock as well as a rapid decline in his clinical state, a transthoracic echocardiogram was done to rule out a cardiac cause of his hypoxia. This revealed a flail mitral valve leaflet with severe mitral regurgitation (Figures 2 and 3; Video). He underwent emergent mitral valve replacement, had an uneventful recovery, and was discharged 2 weeks later.
CASE REPORT
DISCUSSION
A 76-year-old man presented with shortness of breath and cough productive of clear sputum that progressively worsened over 1 day. He denied chest pain, sick contacts, fever, chills, or rigors. On examination, he was anxious and in respiratory distress. His temperature was 96.5 C; respiratory rate was 34 breaths per minute with an oxygen saturation of 76% on a nonrebreather mask; blood pressure was 93/56 mm Hg, and heart rate was 124 beats per minute. Auscultation revealed right-sided rales and a normal cardiac examination. His laboratory values were significant for a white blood cell count of 22,700/mL with neutrophilic predominance and no bands, lactate of 2.4 mg/dL, creatinine of 1.2 mg/dL, and elevated transaminases. His troponin was 0.13 ng/mL and his brain natriuretic peptide titer was 369 pg/mL. His electrocardiogram was notable for sinus tachycardia with no ischemic changes. His blood gas analysis revealed a pH of 7.00, partial pressure of oxygen (PO2) of 42 mm Hg, partial pressure of carbon dioxide (PCO2) of 26 mm Hg, and a chest radiograph revealed extensive right-sided infiltrate compatible with pneumonia (Figure 1). He was immediately started on vancomycin, ceftriaxone, and azithromycin. Unfortunately, his condition worsened quickly and he was transferred to the intensive care unit,
Unilateral pulmonary edema is a rare clinical phenomenon occurring in only 2% of cardiogenic pulmonary edema.2 Due to this low incidence it is usually missed, causing initiation of wrong treatment or delay in appropriate treatment in up to 33% of cases.2,3 This delay contributes to an almost 7-fold increase in mortality when compared with patients presenting with bilateral pulmonary edema.2 Disease entities and factors that could mimic or cause unilateral pulmonary edema include pneumonia (including aspiration), patient positioning, bronchial or pulmonary vein obstruction, pulmonary contusion or infarction, alveolar hemorrhage, or malignancy.4,5 Unilateral pulmonary edema
To the Editor:
Funding: None. Conflict of Interest: None. Authorship: All authors had access to the data and a role in writing this manuscript. Requests for reprints should be addressed to Gbolahan Ogunbayo, MD, Department of Internal Medicine, Rochester General Hospital, 1425 Portland Avenue, Rochester, NY 14621. E-mail address: [email protected]
0002-9343/$ -see front matter Ó 2015 Elsevier Inc. All rights reserved.
Figure 1
Chest radiograph (AP view) at presentation.
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The American Journal of Medicine, Vol 128, No 6, June 2015
Figure 2 Two chamber view of transesophageal echocardiogram Showing the Flail posterior leaflet (pMV) the normal anterior leaflet (aMV) and the Ruptured chordae. The Atrial appendage (AA) is shown.
Figure 3 Color Doppler (Long axis view) of transesophageal Echocardiogram showing the flail posterior leaflet (pMV), normal anterior leaflet (aMV) and the direction of the regurgitant jet (RJ).
is commonly found in patients with acute mitral regurgitation, as in our patient.2,4 This is thought to happen due to the direction of regurgitant blood to the upper branch of the right pulmonary vein.5 This causes a localized increase in hydrostatic pressure.5 Other possible mechanisms are increased capillary permeability, lymphatic obstruction, and increased plasma oncotic pressure.5 Predilection for the right pulmonary vein is due to a higher susceptibility of the thinner posterior leaflet to rupture, directing the regurgitant jet toward the right pulmonary vein.6 It is especially important to distinguish this entity from shock caused by pneumonia, as the treatment for both conditions are different.
specification as well as Sara Catalano, LMSW, who helped proof-reading the manuscript.
Gbolahan O. Ogunbayo, Sumangaly Thambiaiyah, Amole O. Ojo, Adel Obaji,
MD MD MD MD
Department of Internal Medicine Rochester General Hospital Rochester, NY
http://dx.doi.org/10.1016/j.amjmed.2014.12.016
ACKNOWLEDGMENTS I would like to acknowledge Tunji Sangoleye, PsychD, who helped with augmenting the pictures to meet the journals
References 1. Stout KK, Verrier ED. Acute valvular regurgitation. Circulation. 2009;119:3232-3241. 2. Attias D, Mansencal N, Auvert B, et al. Prevalence, characteristics, and outcomes of patients presenting with cardiogenic unilateral pulmonary edema. Circulation. 2010;122:1109-1115. 3. Shin JH, Kim SH, Park J, et al. Unilateral pulmonary edema: a rare presentation of cardiogenic shock due to acute myocardial infarction. J Korean Med Sci. 2012;27:211-214. 4. Young AL, Langston CS, Schiffman RL, Shortsleeve MJ. Mitral valve regurgitation causing right upper lobe pulmonary edema. Tex Heart Inst J. 2001;28:53-56. 5. McNinch RW, McNamara MJ. An unusual cause of right upper- and mid-zone infiltrates on chest x-ray. Crit Care Resusc. 2007;9:256-258. 6. Lesieur O, Lorillard R, Thi HH, Dudeffant P, Ledain L. Unilateral pulmonary oedema complicating mitral regurgitation: diagnosis and demonstration by transesophageal echocardiogram. Intensive Care Med. 2000;26:466-470.
SUPPLEMENTARY DATA Supplementary video accompanying this article can be found in the online version at http://dx.doi.org/10.1016/j. amjmed.2014.12.016.
‘Atypical Pneumonia’: Acute Mitral Regurgitation Presenting with Unilateral Infiltrate
Acute mitral regurgitation is a medical and surgical emergency. It rapidly leads to cardiogenic shock and death if not promptly treated.1
where he was intubated due to worsening hypoxia. He also required 5 vasopressors for blood pressure support. Due to the refractory nature of his shock as well as a rapid decline in his clinical state, a transthoracic echocardiogram was done to rule out a cardiac cause of his hypoxia. This revealed a flail mitral valve leaflet with severe mitral regurgitation (Figures 2 and 3; Video). He underwent emergent mitral valve replacement, had an uneventful recovery, and was discharged 2 weeks later.
CASE REPORT
DISCUSSION
A 76-year-old man presented with shortness of breath and cough productive of clear sputum that progressively worsened over 1 day. He denied chest pain, sick contacts, fever, chills, or rigors. On examination, he was anxious and in respiratory distress. His temperature was 96.5 C; respiratory rate was 34 breaths per minute with an oxygen saturation of 76% on a nonrebreather mask; blood pressure was 93/56 mm Hg, and heart rate was 124 beats per minute. Auscultation revealed right-sided rales and a normal cardiac examination. His laboratory values were significant for a white blood cell count of 22,700/mL with neutrophilic predominance and no bands, lactate of 2.4 mg/dL, creatinine of 1.2 mg/dL, and elevated transaminases. His troponin was 0.13 ng/mL and his brain natriuretic peptide titer was 369 pg/mL. His electrocardiogram was notable for sinus tachycardia with no ischemic changes. His blood gas analysis revealed a pH of 7.00, partial pressure of oxygen (PO2) of 42 mm Hg, partial pressure of carbon dioxide (PCO2) of 26 mm Hg, and a chest radiograph revealed extensive right-sided infiltrate compatible with pneumonia (Figure 1). He was immediately started on vancomycin, ceftriaxone, and azithromycin. Unfortunately, his condition worsened quickly and he was transferred to the intensive care unit,
Unilateral pulmonary edema is a rare clinical phenomenon occurring in only 2% of cardiogenic pulmonary edema.2 Due to this low incidence it is usually missed, causing initiation of wrong treatment or delay in appropriate treatment in up to 33% of cases.2,3 This delay contributes to an almost 7-fold increase in mortality when compared with patients presenting with bilateral pulmonary edema.2 Disease entities and factors that could mimic or cause unilateral pulmonary edema include pneumonia (including aspiration), patient positioning, bronchial or pulmonary vein obstruction, pulmonary contusion or infarction, alveolar hemorrhage, or malignancy.4,5 Unilateral pulmonary edema
To the Editor:
Funding: None. Conflict of Interest: None. Authorship: All authors had access to the data and a role in writing this manuscript. Requests for reprints should be addressed to Gbolahan Ogunbayo, MD, Department of Internal Medicine, Rochester General Hospital, 1425 Portland Avenue, Rochester, NY 14621. E-mail address: [email protected]
0002-9343/$ -see front matter Ó 2015 Elsevier Inc. All rights reserved.
Figure 1
Chest radiograph (AP view) at presentation.
e6
The American Journal of Medicine, Vol 128, No 6, June 2015
Figure 2 Two chamber view of transesophageal echocardiogram Showing the Flail posterior leaflet (pMV) the normal anterior leaflet (aMV) and the Ruptured chordae. The Atrial appendage (AA) is shown.
Figure 3 Color Doppler (Long axis view) of transesophageal Echocardiogram showing the flail posterior leaflet (pMV), normal anterior leaflet (aMV) and the direction of the regurgitant jet (RJ).
is commonly found in patients with acute mitral regurgitation, as in our patient.2,4 This is thought to happen due to the direction of regurgitant blood to the upper branch of the right pulmonary vein.5 This causes a localized increase in hydrostatic pressure.5 Other possible mechanisms are increased capillary permeability, lymphatic obstruction, and increased plasma oncotic pressure.5 Predilection for the right pulmonary vein is due to a higher susceptibility of the thinner posterior leaflet to rupture, directing the regurgitant jet toward the right pulmonary vein.6 It is especially important to distinguish this entity from shock caused by pneumonia, as the treatment for both conditions are different.
specification as well as Sara Catalano, LMSW, who helped proof-reading the manuscript.
Gbolahan O. Ogunbayo, Sumangaly Thambiaiyah, Amole O. Ojo, Adel Obaji,
MD MD MD MD
Department of Internal Medicine Rochester General Hospital Rochester, NY
http://dx.doi.org/10.1016/j.amjmed.2014.12.016
ACKNOWLEDGMENTS I would like to acknowledge Tunji Sangoleye, PsychD, who helped with augmenting the pictures to meet the journals
References 1. Stout KK, Verrier ED. Acute valvular regurgitation. Circulation. 2009;119:3232-3241. 2. Attias D, Mansencal N, Auvert B, et al. Prevalence, characteristics, and outcomes of patients presenting with cardiogenic unilateral pulmonary edema. Circulation. 2010;122:1109-1115. 3. Shin JH, Kim SH, Park J, et al. Unilateral pulmonary edema: a rare presentation of cardiogenic shock due to acute myocardial infarction. J Korean Med Sci. 2012;27:211-214. 4. Young AL, Langston CS, Schiffman RL, Shortsleeve MJ. Mitral valve regurgitation causing right upper lobe pulmonary edema. Tex Heart Inst J. 2001;28:53-56. 5. McNinch RW, McNamara MJ. An unusual cause of right upper- and mid-zone infiltrates on chest x-ray. Crit Care Resusc. 2007;9:256-258. 6. Lesieur O, Lorillard R, Thi HH, Dudeffant P, Ledain L. Unilateral pulmonary oedema complicating mitral regurgitation: diagnosis and demonstration by transesophageal echocardiogram. Intensive Care Med. 2000;26:466-470.
SUPPLEMENTARY DATA Supplementary video accompanying this article can be found in the online version at http://dx.doi.org/10.1016/j. amjmed.2014.12.016.
